In:
International Journal of Cancer, Wiley, Vol. 119, No. 10 ( 2006-11-15), p. 2339-2346
Abstract:
Multiple investigations of the effects of peroxisome proliferator‐activated receptor γ (PPARγ) ligands on colon cancer have produced contradictory results. While some studies demonstrated increased numbers of colonic polyps in Apc Min/+ mice treated with various thiazolidinedione (TZD) PPARγ ligands, others reported amelioration of tumor multiplicity and progression in both Apc Min/+ mice and in mice with chemically‐induced colon cancer. Here, we addressed the role of PPARγ in murine intestinal tumorigenesis using gene knockout methodology. We found that either heterozygous or homozygous intestinal‐specific PPARγ deficiency enhanced the number of Apc Min/+ tumors in both the small intestine and colon, especially in the colon, where PPARγ deficiency also modulated tumor incidence. Gender significantly affected tumor multiplicity independent of PPARγ genotype. Female Apc Min/+ mice developed more tumors in the small intestine and more tumors overall, whereas male Apc Min/+ mice developed more tumors in the colon. Nevertheless, intestinal PPARγ deficiency enhanced tumorigenesis irrespective of gender. Our results suggest that PPARγ functions as a tumor resistance factor in the mouse intestine and warrant further investigation of the PPARγ‐dependent and independent actions of TZDs in cancer. © 2006 Wiley‐Liss, Inc.
Type of Medium:
Online Resource
ISSN:
0020-7136
,
1097-0215
Language:
English
Publisher:
Wiley
Publication Date:
2006
detail.hit.zdb_id:
218257-9
detail.hit.zdb_id:
1474822-8
